Control of Growth Hormone Release

Excess production of growth hormone by pituitary gland in the body is given the name Acromegaly. The exact cause behind Acromegaly can be benign, noncancerous tumors formed in the pituitary gland. Middle aged adults are more prone to develop acromegaly. It is often diagnosed very late because of its slow and insidious onset. The symptoms varies from swelling of hands and feet to protruded lower jaws, joint pain, and deep voice. Accurate diagnosis is established by elevated level of growth hormone (GH) and Insulin-like Growth Factor I (IGF-1) in the blood.

00:01
Let’s now move on to growth hormone.
00:04
Growth hormone, a couple of things here.
00:07
The way that this is setup is the following.
00:09
We’ll begin with the hypothalamus with our
releasing hormone/inhibiting hormone.
00:14
We’ll move from the hypothalamus into the
anterior pituitary.
00:19
This is then known as your somatotroph.
00:22
Collectively, remember that growth hormone
LH share a common precursor known as somatommamotropinand growth hormone will be released from the
anterior pituitary, works upon the liver whereit then releases your insulin-like growth
factor.
00:40
On your left, you’ll notice the following.
00:43
Remember that growth hormone is something
that’s released more so at night when oneis sleeping.
00:49
So, therefore, that pulsatile nature making
growth hormone measurement not the most reliableand also, the growth hormone is a stress hormone.
01:01
With that said, please look at the stimuli
on your left.
01:04
We have sleep… big time; exercise… when
you exercise, you’re consuming glucose.
01:12
Hypoglycaemia, amino acids… all of these
will be triggers for the hypothalamus to releasegrowth hormone releasing hormone.
01:22
On the other side of things, we have growth
hormone inhibiting hormone.
01:25
Please take a look at the key over to your
far right and you’ll notice somatostatin.
01:30
Once again I reiterate that growth hormone
inhibiting hormone is also called somatostatin.
01:36
Used to be called, once upon a time, just
to make sure we cover all basis, that insulin-likegrowth factor was called somatomedin.
01:42
So, there are lot of terms here that have
the prefix somato-, somato-, somato-… somatostatin,somtatotroph, somatomedin… mediating your
growth hormone.
01:54
Next ,we are going to travel through our portal
circulation.
01:56
By that, we mean what?From the hypothalamus through this stalk,
through portal vein and we’re entering theanterior pituitary.
02:06
Within the anterior pituitary, what is the
name of the cell and what stain is it thatreleases growth hormone?The name of the cell is somatotroph, it stains
pink or acidophil.
02:22
It’s responsible for releasing growth hormone.
02:27
This will then work upon the liver.
02:30
From the liver, we release our insulin-like
growth factor and this insulin-like growthfactor is going to be responsible for the
vast, vast functioning of our growth hormoneincluding during a child when we’re growing
up into puberty, our linear growth of ourlong bones.
02:50
Keep in mind that the inhibitory or the feedback
mechanism for IGF1 which is the most importantmeasurement laboratory wise of how well our
growth hormone is functioning in our bodyhas a stimulatory effect on your somatostatin.
03:11
Secretion of growth hormone by somatotroph
is regulated by… we talked about growthhormone releasing hormone and somatostatin
a.k.a. growth hormone inhibiting hormone.
03:23
If excessive growth hormone is being secreted,
then as a child, we or the child becomes agiant or gigantism as an adult.
03:36
And if it’s an adult that has excess growth
hormone, obviously referred to as your acromegaly.
03:43
Here, we have excess amounts of somatomedins
are formed by growth hormone coming from theliver.
03:52
It’s important that you know that somatomedin
exhibits or exerts its inhibitory effect onyour growth hormone by stimulating somatostatin.
04:03
Negative feedback signals are overridden during
sleep when growth hormone levels are highest.
04:10
That is important for you to take out of this
section.
04:14
Hence, the pulsatile nature and the fact that
growth hormone has a shorter half-life thanIGF1 making it a less reliable laboratory
indicator.
04:28
The target organ is the following.
04:30
Let me set this up… of the growth hormone
IGF1 combination.
04:37
The combination of the two or each separately
has different effects, as we shall see.
04:44
Let’s begin.
04:46
Target hypothalamus releasing your growth
hormone releasing hormone works in the anteriorpituitary releasing growth hormone, out comes
the growth hormone.
04:54
The growth hormone has a couple of things.
04:56
Remember, this is stress hormone.
04:58
So, therefore, you are then going to breakdown
your lipid… lipolysis hence releasing yourfree fatty acids.
05:05
You are also going to release your ketones
from your muscle, you’re going to releaseglucose.
05:11
Remember what are we doing here?We are making sure that we do everything in
our power to take those cells that are goingto give us the precursors for gluconeogenesis
biochemically, aren’t we, and for proteinsynthesis.
05:25
So, it’s going to take all of this from
our adipocytes, our liver and muscle and thenplace it into circulation, hence the green
tube that you see here.
05:37
The green tube represents the circulation
and from the circulation, you’ll noticehere the somatomedin means what?Insulin-like growth factor, coming from where?The liver, is then responsible for growth.
05:53
It’s responsible for linear growth of your
long bones, as you see here; it’s responsiblefor protein synthesis, as you can see here;
and to build everything up of your viscera.
06:10
Everything is growing and this is mostly due
to the effect of IGF1, insulin-like growthfactor.
06:19
Here, it’s showing you growth hormone working
up upon your adipocytes resulting in lipolysis.
06:32
Here, from the liver growth hormone works
through gluconeogenesis being the biochemicalpathway.
06:42
Growth hormone from the liver is going to
release insulin-like growth factor 1.
06:48
From the muscle, remember, it wants to have
or bring in those amino acids, it’s theprecursor uptake protein synthesis by growth
hormone and IGF.
07:01
Here, through the action of IGF, you will
have linear bone growth, you’ll have proteinsynthesis and you have a visceral maturity.
07:12
All of these would be through the actions
of somatomedin.
07:15
Prior to all these was the effect of growth
hormone on different cells and tissues…adipocytes, muscles cells and liver.
07:25
Somatomedin, bone growth, on your viscera…growth.
07:34
Without any of this, we have the following
issues.
07:37
In the middle, we have a normal child at the
age of approximately 13.
07:43
On your left is a patient who doesn’t have
growth hormone and this is what’s calledas Lorain levi.
07:54
On your right, you also find a suboptimal
patient with a growth hormone and this iscalled Frohlich’s dwarf.
08:03
Of all the three patients and of the two that
have growth hormone dysfunction, you’llnotice that Lorain levi are those patients
that seem to be the or have the shortest defector the shortest growth.
08:19
So, what’s happening here with Lorain levi?It’s the fact that there’s an actual problem
within your growth hormone receptor.
08:28
If the receptors do not ever function, then
what do you know about the precursor hormoneor the hormone prior?It’s always elevated.
08:38
Deficiency or absence of somatotroph cells,
underproduction of growth hormone, delayedskeletal growth and retarded sexual development,
but alert, intelligent, well proportionalchild.
08:51
IQ perfectly okay, however as far as growth
is concerned, it is completely retarded.
08:59
Now, when you have Frohlich… in Frohlich,
the problem is the following.
09:06
A destructive disease of part of the anterior
pituitary and usually with damage to posteriorpituitary as well and that usually will help
you a little bit more.
09:15
There’s going to be decreased production
of growth hormone and because the anteriorpituitary might be affected during development;
if the thyroid hormones have been affected,there’s going to be the most important statement
here apart from the fact that there’s goingto be stunting of growth and mental-mental
sub-normal or sub-optimal mental activity.
09:42
We did not see this with Lorain levi type
of growth hormone dysfunction.
09:48
Obesity and large appetite for sugar; if atrophy
of other endocrine glands, signs of deficiencyof their hormone.
09:55
So, with Frohlich, you’re thinking about
your anti-pituitary being more of an issue;with Lorain levi, you’re thinking more about
your growth hormone receptor being an issue.
10:06
Know growth hormone in great detail.
10:09
What if it was growth hormone excess?As a kid, there’s gigantism, pretty straight-forward…
long bones over grow as epiphyseal platesare yet diffused.
10:20
As an adult, known as acromegaly, there might
be soft tissue growth, there will be visceromegaly.
10:26
There might be prognathism, the jaw that I
talked about being extremely pronounced andincreased cardiovascular mortality with reduced
life expectancy in non-cured individuals.
10:38
Because there’s visceromegaly as well, “Hey
doc, my hat size is increasing.”Now, with that said, that gives you a couple
differentials, I’ll just name a few.
10:47
Sure, it could be acromegaly, it could also
be Paget’s disease of the bone or it couldbe something like osteopetrosis.
10:55
Okay, so, the three major complaints or-or
the expression of hat size increasing onceagain would be acromegaly and Paget’s disease
of the bone.
11:08
Those are the two big ones, then we’ll get
into orthopaedics, we’ll talk about Paget’sdisease of the bone further so that you clearly
distinguish acromegaly from this and the otherone technically that might also have increased
hat size includes osteopetrosis.

About the Lecture

The lecture Control of Growth Hormone Release by Carlo Raj, MD is from the course Pituitary Gland Disorders.

Included Quiz Questions

IGF is released from the _______ after binding of _______?

Liver; GH

Anterior pituitary; GHRH

Anterior pituitary; GH

Liver; GHRH

Liver; GHIH

Downregulation of GH release involves all EXCEPT which of the following?

GHRH

Somatostatin

Somatomedin

IGF

GHIH

When is GH release pulsatile and at it's highest?

During sleep

During stress

With increased IGF

In the presence of hypoglycemia

When amino acids are low

GH is responsible for stimulating all EXCEPT which of the following?

Breakdown of skeletal muscle into ketones

Lipolysis

Protein synthesis

Gluconeogenesis

IGF secretion from the liver

A child has low levels of IGF and GH. Which presentation would make a diagnosis of Frolich's dwarf more likely?

Subnormal mental maturation

Absence of somatotroph cells

Delayed skeletal growth

Delayed sexual maturation

Subnormal growth

Which of the following is NOT a trigger for the hypothalamus to release GHRH?

Dyslipidemia

Sleep

Exercise

Hypoglycemia

Amino acids

Author of lecture Control of Growth Hormone Release

Carlo Raj, MD

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